Barbiturates transiently block open ACh-activated endplate channels. Barbiturates and other anticonvulsants prolong GABA-activated chloride conductances, whereas convulsants diminish synaptic chloride-dependent responses. Barbiturates also reverse convulsant block of GABA responses. Thus the clinical action of all these drugs may reflect blockage of synaptic ion channels. Blockage of chloride channesl may be of a partially-occluding type, so that under non-equilibrium conditions the synaptic action may be intensified. Mammalian sympathetic ganglia provide ideal material for testing this hypothesis, since they carry both ACh-activated cation channels and GABA-activated anion channels, and are much more similar to human central neurones than muscles offrogs or invertebrate cells. The actions of these drugs on synaptic membrane will be characterize using intracellular recording and iontophoretic and bath application, in experiments modelled on those already successful in muscle.